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Restoration of type I interferon signaling in intrahepatically primed CD8+ T cells promotes functional differentiation.
Kawashima, Keigo; Isogawa, Masanori; Onishi, Masaya; Baudi, Ian; Saito, Satoru; Nakajima, Atsushi; Fujita, Takashi; Tanaka, Yasuhito.
Afiliación
  • Kawashima K; Department of Virology and Liver Unit, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
  • Isogawa M; Department of Gastroenterology and Hepatology, Yokohama City University School of Medicine, Yokohama, Japan.
  • Onishi M; Department of Virology and Liver Unit, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
  • Baudi I; Department of Immunology, National Institute of Infectious Diseases, Tokyo, Japan.
  • Saito S; Department of Virology and Liver Unit, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
  • Nakajima A; Department of Gastroenterology/Internal Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
  • Fujita T; Department of Virology and Liver Unit, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
  • Tanaka Y; Department of Gastroenterology and Hepatology, Yokohama City University School of Medicine, Yokohama, Japan.
JCI Insight ; 6(3)2021 02 08.
Article en En | MEDLINE | ID: mdl-33400688
Hepatitis B virus-specific (HBV-specific) CD8+ T cells fail to acquire effector functions after priming in the liver, but the molecular basis for the dysfunction is poorly understood. By comparing the gene expression profile of intrahepatically primed, dysfunctional HBV-specific CD8+ T cells with that of systemically primed, functional effector counterparts, we found that the expression of interferon-stimulated genes (ISGs) is selectively suppressed in the dysfunctional CD8+ T cells. The ISG suppression was associated with impaired phosphorylation of STAT1 in response to IFN-α treatment. Importantly, a strong induction of type I interferons (IFN-Is) in the liver facilitated the functional differentiation of intrahepatically primed HBV-specific CD8+ T cells in association with the restoration of ISGs' expression in the T cells. These results suggest that intrahepatic priming suppresses IFN-I signaling in CD8+ T cells, which may contribute to the dysfunction. The data also suggest a therapeutic value of the robust induction of intrahepatic IFN-Is for the treatment of chronic HBV infection.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Interferón Tipo I / Virus de la Hepatitis B / Linfocitos T CD8-positivos Límite: Animals / Humans / Male Idioma: En Revista: JCI Insight Año: 2021 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Interferón Tipo I / Virus de la Hepatitis B / Linfocitos T CD8-positivos Límite: Animals / Humans / Male Idioma: En Revista: JCI Insight Año: 2021 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Estados Unidos